Work

Deconstructing endothelial dysfunction: soluble guanylyl cyclase oxidation and the NO resistance syndrome

Year: 2006

Type: article

Abstract: In this issue of the JCI, Stasch and colleagues suggest that a novel drug, BAY 58-2667, potently activates a pool of oxidized and heme-free soluble guanylyl cyclase (sGC; see the related article beginning on page 2552). The increased vasodilatory potency of BAY 58-2667 the authors found in a number of animal models of endothelial dysfunction and in human blood vessels from patients with diabetes suggests that there exists a subphenotype of endothelial dysfunction characterized by receptor-level NO resistance. Diseases associated with NO resistance would appear to be ideally suited for therapies directed at restoring redox homeostasis, sGC activity, and NO sensitivity.

Source: Journal of Clinical Investigation

DOI: 10.1172/jci29807

Author: Mark T. Gladwin

Institutions: National Institutes of Health, National Heart, Lung, and Blood Institute, National Institutes of Health Clinical Center

Language: English

Topic: Nitric Oxide and Endothelin Effects

Subfield: Physiology (medical)

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: green

OpenAlex ID: W1986547098

FWCI: 3.188

Cites: 22

Cited by: 84

Related to: 10